C-type lectin, clec-67, relies on FSHR-1 to function in the innate immune response of C. elegans

C-type lectin, clec-67, relies on FSHR-1 to function in the innate immune response of C. elegans

Jonathan HibshmanAdvisor - Jennifer Powell

The innate immune response is the first line of response to infection. The roundworm, Caenorhabditis elegans, is an excellent model for studying the innate immune response. The G-protein coupled receptor FSHR-1 plays a role in the immune response of worms; however, little is known about the pathway in which it acts. In this work, we show that c-type lectin, clec-67, acts downstream of FSHR-1. C-type lectins are calcium-dependent, carbohydrate binding receptors with a conserved immune function – likely the recognition of pathogen associated glycosilation. Using a clec-67p::GFP reporter we find clec-67 is expressed intestinally in worms with the highest levels of expression at the anterior and posterior segments of the intestine. Further, expression is induced upon infection with Pseudomonas aeruginosa. Silencing FSHR-1 via RNAi reduces the expression levels of clec-67, suggesting it acts in an FSHR-1 dependent manner. However, clec-67 is also regulated directly by GATA transcription factor ELT-2. Thus, FSHR-1 may directly regulate ELT-2 or the pathway may converge with other known immune response pathways for regulating clec-67.